Childhood idiopathic thrombocytopenic purpura associated with human parvovirus B19 infection

Hida, Mariko; Shimamura, Yasushi; Ueno, Etushi; Watanabe, Jun

doi:10.1046/j.1442-200x.2000.01297.x

Cited by 8 publications

(5 citation statements)

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“…In context with acute B19V‐infection, Fanconi anaemia became apparent in patients A2 and A3 and patient A4 developed clinically apparent aplastic anaemia without an underlying condition. Furthermore, B19V‐infection is known to cause thrombocytopenia and to trigger autoimmune disorders [5,20–24]. We observed markers for acute or recent B19V‐infection in five patients presenting with autoimmune disease: ITP was diagnosed in patients AI and AII, Kawasaki‐disease in patient AIII, thrombocytopenia in patient AIV and Evan’s syndrome in patient A1, even though, contraversially, Kawasaki‐disease and Evan’s syndrome have been associated with B19V‐infection [25–27].…”

Section: Discussionmentioning

confidence: 99%

Impact of parvovirus B19 infection on paediatric patients with haematological and/or oncological disorders

Jitschin

Peters

Plentz

et al. 2011

Clinical Microbiology and Infection

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To determine the frequency and the impact of parvovirus B19 (B19V) infection and its influence on the course of haematological and/or oncological diseases in paediatric patients, consecutive serum and bone marrow samples from 110 were analyzed for markers of acute, past and persistent B19V-infection using qPCR, ELISA and WesternLine. Twenty-seven out of 110 (24.5%) children suffered from non-malignant diseases (anaemia, pancytopenia, autoimmune disorders); 68/110 (61.8%) patients had developed leukaemia, malignant lymphoma or solid malignant tumours; 15/110 patients (13.6%) presented with other symptoms. At admission, B19V-specific IgM and IgG indicating acute or previous B19V-infection were observed in 5 (4.5%) and 48 patients (43.6%), respectively. B19V-DNA (10(3) -10(9) geq/mL) was detectable in serum and/or bone marrow of 22 patients (20.0%). These suffered from leukaemia (5), non-Hodgkin lymphoma (2), solid tumours (6), autoimmune (4) and haematological (4) disease and fever (1). During clinical observation four further leukaemia patients developed viraemia and persistent B19V-infection was observed in 13/22 DNA-positive patients. Treatment of B19V-DNA-positive cancer patients was associated with more supportive therapy involving erythrocyte and thrombocyte transfusion and/or antibiotic therapy. Acute B19V-infection has been frequently observed in paediatric patients with haematological and/or oncological disease. In patients with non-malignant diseases anaemia or autoimmune disorders were diagnosed in association with B19V-infection. Furthermore, a significant number of cancer patients displayed markers for acute, recent or persistent B19V-infection. This association may be strengthened by frequent treatment with blood products combined with therapeutic immune suppression. In B19V-infected cancer patients supportive therapy was more complex.

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Section: Discussionmentioning

confidence: 99%

Impact of parvovirus B19 infection on paediatric patients with haematological and/or oncological disorders

Jitschin

Peters

Plentz

et al. 2011

Clinical Microbiology and Infection

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“…ITP in childhood has been estimated to be post‐infectious in approximately two thirds of instances. Many different agents have been implicated in the aetiology of this form of ITP, including not only cytomegalovirus (CMV), but also varicella, rubella, mumps, Epstein‐Barr virus, and parvovirus B19, among others (Chanarin & Walford, 1973; Fiala & Kattlove, 1973;Ip & Corner, 1973; Harris et al , 1975; Muntendam, 1975; Dor et al , 1977; Sahud & Bachelor, 1978; Shimm et al , 1980; Aguado et al , 1984; Anton et al , 1985; Amitai & Granit, 1986; Landonio et al , 1992; Wright, 1992; Eisenberg & Kaplan, 1993; Murray et al , 1994; Mizutani et al , 1995; Von Spronsen & Breed, 1996; Wright et al , 1996; Arruda et al , 1997; Miyahara et al , 1997; Swanobori et al , 1997; Gasbarrini et al , 1998; Gural et al , 1998; Lopez et al , 1998; Heegaard et al , 1999; Sakata et al , 1999; Aboulafia et al , 2000; Crapnell et al , 2000; Garcia‐Suarez et al , 2000; Hida et al , 2000; Hsiao, 2000; Emilia et al , 2001; Scaradavou, 2002; Yenicesu et al , 2002; Ichiche et al , 2003; Aktepe et al , 2004; Alliot & Barrios, 2005; Jackson et al , 2005; Li et al , 2005; Nomura et al , 2005; Rajan et al , 2005; Asahi et al , 2006; Cooper & Bussel, 2006; Sayan et al , 2006; Suvajdzic et al , 2006). These infections trigger an autoimmune process against platelets, even though the infections themselves are transient and seemingly neither atypical or severe in nature.…”

Section: Findings In Reported Cases Of Cmv‐related Itp*mentioning

confidence: 99%

Cytomegalovirus can make immune thrombocytopenic purpura refractory

2009

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SummaryImmune thrombocytopenic purpura (ITP) is characterized by decreased platelet numbers secondary to platelet destruction and reduced platelet production. Even if the ITP persists, it typically responds to 'ITP-specific' therapies, such as intravenous immunoglobulin, steroids, intravenous anti-D, and splenectomy. Several reports, including our previous study, have implicated cytomegalovirus (CMV) in the pathogenesis of infrequent cases of ITP that were not severe in nature. A recent study from China suggested that CMV is the aetiology of some cases of acute ITP of childhood and may require different treatment. We report two adult and two paediatric patients with refractory, severe, symptomatic thrombocytopenia, who were diagnosed with ITP and found to have active CMV infection. Their presentations included fever, transaminitis, neutropenia, and atypical lymphocytosis, but in particular, treatment-refractory, severe ITP. Treatment with steroids appeared to worsen the CMV-ITP. All four cases showed improvement in platelet counts within two weeks of starting ganciclovir and cytogam and tapering steroids. Based on the four patients described here, we believe that, in certain cases, CMV infection will result in symptomatic, severe, refractory ITP, which may be indistinguishable from typical ITP. Eradication of CMV with antiviral therapy improved the ITP in these cases.

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“…The virus is now also known to cause transient aplastic crisis (TAC) in hereditary spherocytosis and fetal hydrops in early pregnancy 2 . In addition, B19 has been reported to cause a wide variety of diseases: diseases mainly characterized by purpura, such as Henoch–Schönlein purpura, idiopathic thrombocytopenic purpura, thrombotic thrombocytopenic purpura, and papular‐purpuric gloves and socks syndrome (PPGSS); diseases suggestive of collagen diseases, such as lupus‐like syndrome and rheumatoid arthritis, and severe acute diseases such as hemophagocytic syndrome (HPS) 3–8 . However, no studies have sequentially quantified serum viral DNA for comparison among these diseases.…”

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confidence: 99%

Quantitation of human parvovirus B19 DNA by real‐time polymerase chain reaction

Takano

Yamada

2007

Pediatrics International

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The amount of parvovirus B19 DNA correlated well with the stage of infection, and its quantitation was useful for determining disease status and prognosis. In parvovirus B19 infection, the viremia is associated with rare but varied pathological states different from erythema infectiosum, such as transient aplastic crisis, hemophagocytic syndrome, lupus-like syndrome, and papular-purpuric gloves and socks syndrome.

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Childhood idiopathic thrombocytopenic purpura associated with human parvovirus B19 infection

Cited by 8 publications

References 0 publications

Impact of parvovirus B19 infection on paediatric patients with haematological and/or oncological disorders

Impact of parvovirus B19 infection on paediatric patients with haematological and/or oncological disorders

Cytomegalovirus can make immune thrombocytopenic purpura refractory

Quantitation of human parvovirus B19 DNA by real‐time polymerase chain reaction

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